Despite the unprecedented success of immune checkpoint blockade (ICB) and molecular-targeted therapy in other types of cancer, the vast majority of patients with PDAC have failed to benefit from these treatment methods, apart from a minority of patients with microsatellite instability or KRAS-G12C mutation, features associated with a better response to ICB [2–4] or KRAS-G12C-specific inhibitors [5]. This evidence concerns the gene KRAS and cancer.